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Abstract
BackgroundThe aim of this study was to investigate the oncogenic function and regulatory mechanism of stathmin in oral squamous cell carcinoma (OSCC).MethodsTwo-dimensional electrophoresis and liquid chromatography-tandem mass chromatography were applied to screen differentiated proteins during carcinogenesis in OSCC. Cell Counting Kit-8 (CCK-8) assays, colony formation, migration, flow cytometry, immunofluorescence and a xenograft model were used to detect the function of stathmin. The correlation between stathmin and p53 expression was analyzed using immunohistochemistry. Mutant/wild type p53 plasmids and small interfering RNA were used to examine the regulation of stathmin. Chromatin immunoprecipitation assays and luciferase assays were performed to detect the transcriptional activation of stathmin by p53.ResultsOverexpression of stathmin was screened and confirmed in OSCC patients and cell lines. Silencing expression of stathmin inhibited proliferation, colony formation and migration and promoted apoptosis. Poly ADP ribose polymerase (PARP) and cyclin-dependent kinase 1 (cdc2) were activated after silencing the expression of stathmin. Suppression of tumorigenicity was also confirmed in vivo. Mutant p53 transcriptionally activated the expression of stathmin in HN6 and HN13 cancer cells, but not in HN30 cells harboring wild type p53.ConclusionsThese results suggest that stathmin acts as an oncogene and is transcriptionally regulated by mutant p53, but not by wild-type p53. Stathmin could be a potential anti-tumor therapeutic target in OSCC.
Highlights
The aim of this study was to investigate the oncogenic function and regulatory mechanism of stathmin in oral squamous cell carcinoma (OSCC)
Stathmin was overexpressed during carcinogenesis of immortalized oral epithelial cells to squamous carcinoma cells (Fig. 1c–f)
When Small interfering RNA (siRNA) against p53 was transfected into the two mutp53 cell lines, HN6 (H179L) and HN13 (V173 L), we found decreased stathmin expression accompanied by p53 knockdown at both the protein and mRNA levels (Fig. 6c, e)
Summary
The aim of this study was to investigate the oncogenic function and regulatory mechanism of stathmin in oral squamous cell carcinoma (OSCC). Oral squamous cell carcinoma (OSCC) accounts for more than 300,000 new cases each year and has poor clinical outcomes with a 5-year survival rate of only 50–60%, which is even lower in patients with locally advanced disease [1, 2]. Despite substantial progress made in the past few decades to understand the mechanism of carcinogenesis, treatment strategy has developed slowly for OSCC. Surgery remains the best option for OSCC patients but it is not effective on late-stage metastatic tumors [3]. It is crucial to deeply investigate the molecular network involved in gain-of-function (GOF) mutations of p53 in OSCC
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